Hyperbaric oxygen therapy (HBOT) is used to diminish the size of
the bubbles, not simply through pressure, but also by using an
oxygen gradient. According to Boyle’s law, the volume of the bubble
becomes smaller as pressure increases. With a change in 1.8 ATA,
this is only about 30%. The bubble causing DCS is thought to be
composed of nitrogen. When a tissue compartment is at equilibrium
and then ascends to a decreased atmospheric pressure, nitrogen seeps
out of blood, tissue, or both, causing a bubble. During HBOT, the
patient breathes 100% oxygen, creating oxygen-rich, nitrogen-poor
blood. This creates a gradient of nitrogen between the blood and the
bubble, causing nitrogen to efflux from the bubble into the
bloodstream, which, in effect, makes the bubble smaller.[25]

The treatment of choice is recompression. Although treatment as
soon as possible has the greatest success, recompression is still
the definitive treatment, and no exclusionary time from symptom
onset has been established.[25,
26] DCS Type I can be treated using the
US Navy Treatment Table 5: 60 fsw for two 20-min periods, with a
slow decompression to 30 fsw for another 20 minutes. For DCS types
I, II, and III, the
US Navy Treatment Table 6 is a recommended treatment protocol.
Patients are placed at 60 fsw (2.8 ATA) for at least three 20-min
intervals and then are slowly decompressed to 30 fsw. They remain
there for at least another 2.5 hours. The time a patient is kept at
60 or 30 fsw can be extended depending on the patient’s symptom
response to therapy.[28]

Air Embolism

Air embolism refers to bubbles in the arterial or venous
circulation. Venous bubbles can result from compressed gas diving
(such as scuba)[29]
but are often filtered through the pulmonary capillary
bed. If a large volume of bubbles is noted, they may overwhelm the
pulmonary filter and enter the arterial circulation.[30]
Arterial gas emboli (AGE) can also result from pulmonary
barotrauma[25]
or accidental intravenous air injection or some surgical
procedures.[31,
32, 33, 34, 35] Symptoms usually occur within seconds to
minutes of the event and can include loss of consciousness,
confusion, neurological deficits, cardiac arrhythmias, or cardiac
arrest.

The treatment of choice is recompression therapy. Gas embolism
used to be treated with US Navy Treatment Table 6A, which required a
pressure of 6 ATA. The rationale was that the larger volume of gas
warranted increased pressure to force bubble redistribution or
elimination. No conclusive evidence shows that this offers superior
treatment to the US Navy Treatment Table 6 for most cases; however,
if complete relief is not achieved after initial recompression,
deeper recompression may be needed.[25]

CO binds to hemoglobin with 200 times the affinity of oxygen. CO
also shifts the oxygen dissociation curve to the left (the Haldane
effect), which decreases oxygen release to tissues. CO can also bind
cytochrome oxidase aa3/C and myoglobin. Reperfusion injury can occur
when free radicals and lipid peroxidation are produced.

The treatment of CO poisoning with hyperbaric oxygen therapy
(HBOT) is based upon the theory that oxygen competitively displaces
CO from hemoglobin. While breathing room air, this process takes
about 300 minutes. While on a 100% oxygen nonrebreather mask, this
time is reduced to about 90 minutes; with HBOT, the time is
shortened to 32 minutes. HBOT (but not normobaric oxygen) restores
cytochrome oxidase aa3/C[36]
and helps to prevent lipid peroxidation.[37]
HBOT is also used to help prevent the delayed neurologic
sequelae (DNS); treatment instituted sooner is more effective.[38]
Multiple papers describe controversial methods and
conclusions about the use of HBOT for CO poisoning.[39,
37, 40, 41, 42]

Patients with CO poisoning can present with myriad symptoms that
they may not initially attribute to CO poisoning, as CO is
considered the “great imitator” of other illnesses.[18,
43, 44] Presentation can include flulike symptoms such as
headache, visual changes, dizziness, and nausea. More serious
manifestations include loss of consciousness, seizures, chest pain,
ECG changes, tachycardia, and mild to severe acidosis.

Candidates for HBOT are those who present with morbidity and
mortality risks that include pregnancy and cardiovascular
dysfunction and those who manifest signs of serious intoxication,
such as unconsciousness (no matter how long a period), neurologic
signs, or severe acidosis. CO-hemoglobin (Hgb) level usually does
not correlate well with symptoms or outcome;[45,
37, 46] many patients with CO-Hgb levels of 25-30% are
treated.

Pregnant females often have a CO level that is 10-15% lower than
the fetus. Fetal Hgb not only has a higher affinity for CO but also
has a left-shifted oxygen dissociation curve compared with adult
hemoglobin. Exposure to CO causes an even farther leftward shift, in
both adult and fetal hemoglobin, and decreased oxygen release from
maternal blood to fetal blood and from fetal blood to fetal tissues.
Pregnant patients with CO-Hgb levels greater than 10% should be
treated with HBOT.[2]

HBOT is administered at 2.5-3 ATA for periods of 60-100 minutes.
Depending on patient presentation and response, 1-5 treatments are
recommended.[3]

Enhancement of Healing in Selected Problem Wounds

Normal wound healing proceeds through stages of hemostasis,
removal of infectious agents, resolution of the inflammatory
response, reestablishment of a connective tissue matrix,
angiogenesis, and resurfacing.
Problem (or chronic) wounds are those which do not proceed
completely through this process because of any number of local and
systemic host factors. For this reason, chronic wounds are often
categorized as diabetic wounds, venous stasis ulcers, arterial
ulcers, or
pressure ulcers.

Wounds that fail to heal are typically hypoxic.[47]
Multiple components of the wound healing process are
affected by oxygen concentration or gradients, which explains why
hyperbaric oxygen therapy (HBOT) can be an effective therapy to
treat chronic wounds. Angiogenesis occurs in response to high oxygen
concentration.[10]
This is likely a multifactorial effect of HBOT. First,
fibroblast proliferation and collagen synthesis are oxygen
dependent,[11]
and collagen is the foundational matrix for angiogenesis.
In addition, HBOT likely stimulates growth factors involving
angiogenesis and other mediators of the wound healing process.[48]
Hyperbaric oxygen also has been shown to have direct and
indirect antimicrobial activity; in particular, it increases
intracellular leukocyte killing.[13,
14, 12]

Diabetic lower extremity ulcers have been the focus of most wound
research in hyperbaric medicine, since the etiology of these wounds
is multifactorial, and HBOT can address many of these factors.
Several randomized controlled clinical trials have studied HBOT for
the treatment of diabetic lower extremity wounds.[49,
50, 51, 52] Additionally, many more prospective,
noncontrolled clinical trials and retrospective trials have been
completed. Based on the body of evidence, major insurance carriers
around the world now endorse the use of HBOT for the treatment of
diabetic lower extremity wounds that show evidence of deep soft
tissue infection, osteomyelitis, or gangrene. HBOT has been shown to
reduce the amputation rate in patients with diabetic ulcers as well.[49,
50, 52]

In an effort to select patients appropriately for HBOT, various
objective vascular evaluation methods have been used, including
transcutaneous oximetry, capillary perfusion pressure, laser
Doppler, and other types of vascular studies. Debate is ongoing
regarding which method provides the most reliable data and whether
these methods are more useful than other clinical markers of wound
failure.

Note that HBOT should be used in conjunction with a complete
wound healing care plan. As with all chronic wounds, other
underlying host factors (eg, large vessel disease, glycemic control,
nutrition, infection, presence of necrotic tissue, offloading) must
be simultaneously addressed in order to have the highest chance of
successful healing and functional capacity.

Because the goals of HBOT for wound healing include cellular
proliferation and angiogenesis, HBOT is generally performed daily
for a minimum of 30 treatments. Treatment is generally at 2 to 2.4
ATA for a total of 90 minutes of 100% oxygen breathing time. Based
on the response to therapy, extended courses of therapy may be
indicated.

Compromised Skin Grafts and Flaps

Most
skin grafts and flaps in normal hosts heal well. In patients
with compromised circulation, this may not be the case. Patients
with diabetes or vasculopathy from another etiology and patients who
have irradiated tissue are particularly subject to flap or graft
compromise. In these patients, hyperbaric oxygen therapy (HBOT) has
been shown to be useful. Unfortunately, if patients are not
identified early, the initial flap or graft may be lost. Even in
such cases, patients can significantly benefit from HBOT to prepare
the wound bed for another graft or flap procedure; the procedure
then has a higher chance of success following HBOT.

Over 30 animal studies have shown efficacy of HBOT in preserving
both pedicled and free flaps in multiple models. These models looked
at arterial, venous, and combined insults in addition to irradiated
tissues. While improvement was observed regardless of the type of
vascular defect, those with arterial insufficiency and radiation
injury showed the greatest improvement.

Human case studies showing benefit of hyperbaric treatment for
flap survival were first reported in 1966. A controlled clinical
trial showing improved survival of split skin grafts followed
shortly thereafter.[53]
This was corroborated by a later clinical trial.[54]
Additionally, evidence exists of benefit for flaps in
post-irradiated tissue in human subjects.[55]

As the underlying pathophysiology of all compromised grafts and
flaps is hypoxia, HBOT benefits patients by reducing the oxygen
deficit. A unique mechanism of action of HBOT for preserving
compromised flaps is the possibility of closing arteriovenous
shunts.[56]
Additionally, the same mechanisms of action that improve
wound healing, namely, improved fibroblast and collagen synthesis[11]
and angiogenesis,[10]
also are likely to benefit a compromised graft or flap.

The current standard for HBOT to treat a compromised graft or
flap includes twice daily treatment until the graft or flap appears
viable and then once per day until completely healed. The initiation
of HBOT should be expedited. In general, benefit should be seen by
20 treatments; if it is not, continuation of therapy should be
reviewed. However, the cost of creating a complex flap is high,
which makes HBOT cost-effective for this diagnosis. Of course,
patients with compromised flaps need surgical attention to the
arterial and venous supply, appropriate local management, and
maximization of medical support.

Crush Injury and Compartment Syndrome

Acute peripheral traumatic ischemia includes those injuries that
are caused by trauma that leads to ischemia and edema; a gradient of
injury exists. This category contains crush injuries as well as
compartment syndrome. Crush injuries often result in poor
outcome because of the body’s attempt to manage the primary injury.
The body then develops more injury due to the reperfusion response.
Injuries are graded using definite points on a severity scale. The
commonly referenced system is the Gustilo classification,[57]
but other classification scales are available.

The benefits of hyperbaric oxygen therapy (HBOT) for this
indication include hyperoxygenation by increasing oxygen within the
plasma. HBOT also induces a reduction in blood flow[58,
59] that allows capillaries to resorb extra fluid,
resulting in decreased edema. As a gradient of oxygenation is based
on blood flow, oxygen tissue tensions can be returned, allowing for
the host defenses to properly function.[11]
Animal studies suggest that a decreased neutrophil
adherence to ischemic venules is observed with elevated oxygen
pressures (2.5 ATA).[15,
16] Reperfusion injury is diminished, as HBOT generates
scavengers to destroy oxygen radicals.[60]

Compartment syndrome also is a continuum of injury that occurs
when compartment pressures exceed the capillary perfusion pressures.
The extent to which the injury has affected tissues is unclear, even
after surgical intervention.[61,
58, 62] HBOT is not recommended during the “suspected”
stage of injury, when compartment syndrome is not yet present but
may be impending. HBOT is beneficial during the impending stage,
when objective signs are noted (pain, weakness, pain with passive
stretch, tense compartment). With these signs, even if surgery is
not elected because of compartment pressures or patient stability,
HBOT is indicated. Once the patient has undergone fasciotomy, HBOT
can be used to help decrease morbidity.[3]

HBOT should be started as soon as is feasible, ideally within 4-6
hours from time of injury. After emergent surgical intervention, the
patient should undergo HBOT at 2-2.5 ATA for 60-90 minutes. For the
next 2-3 days, perform HBOT 3 times daily, then twice daily for 2-3
days, and then daily for the next 2-3 days.[2]

Necrotizing Soft Tissue Infections

These infections may be single aerobic or anaerobic but are more
often mixed infections that often occur as a result of trauma,
surgical wounds, or foreign bodies, including subcutaneous and
muscular injection of contaminated street drugs. They are often seen
in compromised hosts who have diabetes or a vasculopathy of another
type. These infections are named based on their clinical
presentation and include
necrotizing fasciitis,
clostridial and nonclostridial myonecrosis, and
Fournier gangrene.

Regardless of the depth of the tissue invasion, these infections
have similar pathophysiology that includes local tissue hypoxia,
which is exacerbated by a secondary occlusive endarteritis.[63]
Intravascular sequestration of leukocytes is common in
these types of infections, mediated by toxins from specific
organisms.[64]
Clostridial theta toxin appears to be one such mediator.
All of these factors together foster an environment for facultative
organisms to continue to consume remaining oxygen, and this promotes
growth of anaerobes.

The cornerstones of therapy are wide surgical debridement and
aggressive antibiotic therapy. Hyperbaric oxygen therapy (HBOT) is
used adjunctively with these measures, as it offers several
mechanisms of action to control the infection and reduce tissue
loss. First, HBOT is toxic to anaerobic bacteria.[65]
Next, HBOT improves polymorphonuclear function and
bacterial clearance.[12,
66] Based on results of work related to CO poisoning, HBOT
may decrease neutrophil adherence based on inhibition of beta-2
integrin function.[17,
16] Further investigation is needed to see if this
mechanism is at work in necrotizing infections as well. In the case
of clostridial myonecrosis, HBOT can stop the production of the
alpha toxin.[19,
67] Finally, limited evidence indicates that HBOT may
facilitate antibiotic penetration or action in several classes of
antibiotics, including aminoglycosides,[20]
cephalosporins,[22]
sulfonamides[21]
and amphotericin.[23]

Multiple clinical studies suggest that HBOT is efficacious in the
treatment of necrotizing soft tissue infections. These include case
series, retrospective and prospective studies, and non-randomized
clinical trials. They suggest significant reductions in mortality
and morbidity. The reduction in mortality was remarkably similar in
2 studies: 34% (untreated) vs. 11.9% (treated) in one study;[68]
38% (untreated) vs. 12.5% (treated) in the other.[69]
In another study,[70]
the treated group had more patients with diabetes and more
patients in shock and still had significantly less mortality (23%)
than the untreated group (66%). Clinical studies involving patients
with Fournier gangrene treated with HBOT bear similar results.

Initial HBOT is aggressively performed at least twice per day in
coordination with surgical debridement. Typically, a treatment
pressure ranging from 2.0-2.5 ATA is adequate. However, in the
specific case of clostridial myonecrosis, 3 ATA is often used to
ensure adequate tissue oxygen tensions to stop alpha toxin
production. For the same reason, HBOT should be initiated as quickly
as possible in this circumstance and performed 3 times in the first
24 h if at all feasible.

Intracranial abscess

The disorders considered in treatment of intracranial abscesses
(ICA) include subdural and epidural empyema as well as cerebral
abscess.[2]
Studies from around the world have reviewed mortality from
ICA with a resulting mortality of about 20%.[71]
HBOT has multiple mechanisms that make it useful as an
adjunctive therapy for ICA.

HBOT induces high oxygen tensions in tissue, which helps to
prevent anaerobic bacterial growth, including organisms commonly
found in ICA.[72,
73, 74, 75] HBOT can also help reduce increased
intracranial pressure (ICP) and its effects are proposed to be more
pronounced with perifocal brain swelling.[9,
76, 77] As discussed earlier, HBOT can enhance host immune
systems and the treatment of osteomyelitis.[78]
Candidates for adjunctive HBOT are patients who have
multiple abscesses, who have an abscess that is in a deep or
dominant location, whose immune systems are compromised, in whom
surgery is contraindicated, who are poor candidates for surgery, and
who exhibit inadequate response despite standard surgical and
antibiotic treatment.[3]

HBOT is administered at 2.0-2.5 ATA for 60-90 minutes per
treatment. HBOT may be 1-2 sessions per day. The optimized number of
treatments has not been determined.[3]

Delayed Radiation Injury

Radiation therapy causes acute, subacute, and delayed injuries.
Acute and subacute injuries are generally self-limited. However,
delayed injuries are often much more difficult to treat and may
appear anywhere from 6 months to years after treatment. They
generally are seen after a minimum dose of 6000 cGy. While uncommon,
these injuries can cause devastating chronic debilitation to
patients. Notably, they can be quiescent until an invasive procedure
is performed in the radiation field. Injuries are generally divided
into soft tissue versus hard tissue injury (osteoradionecrosis
[ORN]).

While the exact mechanism of delayed radiation injury is still
being elucidated, the generally accepted explanation is that an
obliterative endarteritis and tissue hypoxia lead to secondary
fibrosis.[79]
Hyperbaric oxygen therapy (HBOT) was first used to treat
ORN of the mandible. Based on the foundational clinical research of
Marx,[80]
multiple subsequent studies supported its use. The success
of HBOT in treating ORN then led to its use in soft tissue
radionecrosis as well.

Osteoradionecrosis

Marx demonstrated conclusively that ORN is primarily an avascular
aseptic necrosis rather than the result of infection.[80]
He developed a staging system for classifying and planning
treatment,[81]
which is largely accepted throughout the oromaxillofacial
surgery community.

Stage I - Exposed alveolar bone: The patient receives 30
HBOT treatments and then is reassessed for bone exposure,
granulation, and resorption of nonviable bone. If response
is favorable, an additional 10 treatments may be considered.

Stage II - A patient who formerly was Stage I with
incomplete response or failure to respond: Perform transoral
sequestrectomy with primary wound closure followed by an
additional 10 treatments.

Stage III - A patient who fails stage II or has an
orocutaneous fistula, pathologic fracture, or resorption to
the inferior border of the mandible: The patient receives 30
treatments, transcutaneous mandibular resection, wound
closure, and mandibular fixation, followed by an additional
10 postoperative treatments.

The cornerstone of therapy is to begin and complete (if possible)
HBOT prior to any surgical intervention and then to resume HBOT as
soon as possible after surgery. Only in this way is adequate time
allowed for angiogenesis to support postoperative healing. For
patients with a history of significant radiation exposure, but no
exposed bone, who require oral surgery, many practitioners suggest
20 HBOT treatments prior to surgery and 10 treatments immediately
following surgery. Feldmeier has published an excellent review of
this literature.[82]

Soft tissue radionecrosis

While soft tissue radionecrosis also is rare, it causes
significant morbidity, depending on the site of injury. All of these
injuries lead to significant local pain. Both
radiation cystitis and radiation proctitis can result in severe
blood loss with symptomatic anemia, and radiation cystitis may cause
obstructive uropathy secondary to fibrosis and blood clot formation.
Radionecrosis of the neck and larynx can lead to dysphagia and
respiratory obstruction. Irradiated skin develops painful, necrotic
wounds that do not heal with standard wound healing care plans.

For each of these subpopulations of soft tissue radionecrosis,
published case series and prospective, nonrandomized clinical trials
corroborate one another, providing a degree of external validity.
Larger studies are warranted. A national registry is currently being
evaluated, from which more powerful conclusions may be forthcoming.
Currently, the largest group of reported patients treated with HBOT
for soft tissue radionecrosis are those with radiation cystitis. At
least 15 publications, representing almost 200 patients, report a
combined success rate in the 80% range. The 2 largest studies were
published by Bevers[83]
and Chong.[84]

HBOT and carcinogenesis

Practitioners and patients are often concerned that HBOT may
foster recurrence of malignancy or promote the growth of an existing
tumor. This is largely because of the known angiogenic effective of
HBOT. Feldmeier has reviewed this subject extensively. Malignant
angiogenesis appears to follow a different pathway than angiogenesis
related to wound healing. His review of the literature suggests that
the risk is low.[85]

Refractory Osteomyelitis

Refractory osteomyelitis is defined as acute or chronic
osteomyelitis that is not cured after appropriate interventions.
More often than not, refractory osteomyelitis is seen in patients
whose systems are compromised. This condition often results in
nonhealing wounds, sinus tracts, and, in the worst case, more
aggressive infections that require amputation.

Mader and Niinikoski showed that hyperbaric oxygen therapy (HBOT)
is capable of elevating oxygen tension in infected bone to normal or
above normal levels.[86,
12] Since polymorphonuclear (PMN) function requires
adequate oxygen concentration, this is a significant mechanism by
which HBOT helps to control osteomyelitis, as demonstrated by Mader
in the same study.[12]

A unique mechanism by which HBOT is beneficial in osteomyelitis
is in promoting osteoclast function. The resorption of necrotic bone
by osteoclasts is oxygen-dependent. This has best been demonstrated
in animal models of osteomyelitis.[87]

Additionally, as previously mentioned, HBOT facilitates the
penetration or function of antibiotic drugs. Other properties of
HBOT previously discussed, such as neovascularization and blunting
the inflammatory response, likely provide additional benefit.

Convincing animal evidence supports the use of HBOT in the
treatment of osteomyelitis. Clinical studies are somewhat
problematic, however, because osteomyelitis has so many different
presentations that comparisons become difficult. This is compounded
by the small study sizes found in the literature; however, these do
suggest benefit of HBOT for refractory osteomyelitis in humans.

One specific subset of osteomyelitis that merits special
attention is malignant otitis externa. This progressive pseudomonal
osteomyelitis of the ear canal can spread to the skull base and
become fatal. Davis et al published a study of 17 patients with
malignant otitis externa, all of whom showed dramatic improvement
with the addition of HBOT to standard surgical debridement and
antibiotic therapy.[88]

Thermal Burns

Thermal burns present a multifactorial tissue injury that
culminates in a marked inflammatory response with vascular
derangement from activated platelets and white cell adhesion with
resultant edema, hypoxia, and vulnerability to severe infection.
Poor white cell function caused by the local environment exacerbates
this problem. Hyperbaric oxygen therapy (HBOT) addresses each of
these pathophysiological derangements, and can, therefore, make a
significant difference in patient outcomes. These mechanisms of
action have been discussed above.

Multiple animal studies support the utility of HBOT for treatment
of thermal burns. Human studies ranging from case series to
randomized clinical trials have supported the potential benefit of
HBOT in burn treatment. These include a small randomized study by
Hart[89]
that demonstrated improved healing and decreased
mortality. Niezgoda[90]
showed increased healing in a standardized human burn
model. In a series of publications, Cianci[91,
92] suggests significant reduction in length of hospital
stay, need for surgery, and cost.

Because of the goals of therapy, HBOT is begun as soon as
possible after injury, with a goal of 3 treatments within the first
24 hours and then twice daily. Length of treatment depends on the
clinical impairment of the patient and the extent of and response to
grafting. Special attention must be given to fluid management and
chamber and patient temperature to avoid undue physiologic stress to
the patient as well as potential complications of treatment (ie,
oxygen toxicity).

Exceptional Anemia

Patients who develop exceptional anemia have lost significant
oxygen carrying capacity in the blood. These patients become
candidates for hyperbaric oxygen therapy (HBOT) when they are unable
to receive blood products because of religious or medical reasons.
The major oxygen carrier in human blood is hemoglobin, transporting
1.34 mL of oxygen per gram. Borema performed an experiment in the
1960s in which exsanguinated pigs (who had only plasma in their
vasculature) were able to sustain life under hyperbaric conditions.[5]

The body generally uses 5-6 vol% (mL of O2 per 100 mL
of blood);[93]
under 3 ATA, 6 vol% of molecular oxygen can be dissolved
into the plasma.[94]
The CNS and cardiovascular systems are the two most
oxygen-sensitive systems in the human body.[93,
95] Oxygen debt is one way of determining a patient’s need
to start or continue HBOT. A cumulative oxygen debt is the time
integral of the volume of oxygen consumption (VO2)
measured during and after shock insult minus the baseline VO2
required during the same time interval.[3]
Patients who have a debt >33 L/m2 do not
survive, whereas patients with debts ≤9 usually recover.[2]

HBOT is administered at 2-3 ATA for periods of up to 4 hours per
treatment. As many as 3-4 sessions a day may be necessary, depending
on a patient’s clinical picture. Treatments should continue until
the patient can receive blood products, no longer demonstrates end
stage organ failure, or no longer has a calculated oxygen debt.[3]

Central Retinal Artery Occlusion

Central retinal artery occlusion (CRAO) is a sudden, painless
loss of vision; this is the most recently approved indication by the
Undersea and Hyperbaric Medicine Society (UHMS) for HBOT.[96]
CRAO is caused by the obstruction of the central retinal
artery and, although an infrequent cause of visual loss,[97]
leads to permanent visual loss. Current treatment for CRAO
consists of attempts to lower intraocular pressure and movement of a
potential embolus downstream, ocular massage, anterior chamber
paracentesis, and medications (both eye drops and oral); most
modalities have proven inefficacious.[98]

A small study by Hertzog et al evaluated HBOT with CRAO. Patients
were divided into groups based on time of onset of CRAO to HBOT. The
study noted that HBOT was most useful in preserving vision if
instituted within 8 hours.[99]
Another retrospective study published by Beiran compared
patients from a facility where HBOT was available to a facility that
did not have HBOT. The patients who received HBOT demonstrated
visual improvement (82% HBOT vs 29.7% control).[100]

Patient selection for HBOT should meet the following criteria: <
24 hours of painless vision loss; no history of flashes or floaters
prior to vision loss; visual acuity 20/200 or worse, even with
pinhole testing; age >40 years; and no recent eye surgery or trauma.[96]
Visual improvement has been reported even with delay of
HBOT.[101]

HBOT is administered at 2 ATA on 100% oxygen. If no response is
noted, pressure should be increased to 2.8 ATA. If vision is still
not improved after 20 minutes, US Navy treatment Table 6 is
indicated. If vision is improved, continue at treatment depth for 90
minutes bid. Continue daily bid compression until resulting in 3
days without visual improvement. If the patient responds to 100%
oxygen via nonrebreather (NRB) mask itself, HBOT is not needed, and
the patient should be maintained on surface 100% oxygen for 12
hours.[96]

Complications and Special Concerns

As with any medical therapy, treatment brings both risks and
benefits. One of the more frequently seen injuries caused by
hyperbaric oxygen therapy (HBOT) is barotrauma (ie, injuries caused
by pressure as a result of an inability to equalize pressure from an
air-containing space and the surrounding environment).[2,
3]

Pediatric considerations

Pediatric patients also have special concerns. The proportion of
surface area to body mass is much greater in children than in
adults. As temperature in the chamber can fluctuate, care must be
taken to ensure the child remains warm without causing hyperthermia.
This can be more difficult in a monoplace chamber because the
patient cannot be physically reached from outside the chamber to
provide blankets or warmed water as heat sources. Unless children
can focus and equalize their ears, consideration for placement of
tympanostomy tubes should be discussed with the parents to prevent
middle ear barotrauma.

Oxygen administration is easy in a monoplace chamber because the
chamber is pressurized with oxygen. Multiplace chambers can fashion
equipment to fit the child. A neck ring can be fitted over the
child’s torso, or, if the child is small enough, 2 hoods can be
placed together to form a capsule around the child. Care must be
taken when treating patients with ductal dependent lesions, as
oxygen is a signal for ductus arteriosus closure. This has not been
a documented problem in pregnancy. Bronchopulmonary dysplasia in a
preterm infant, as is associated